Our research elucidated that FOXD1‐AS1 released PIK3CA by sponging miR‐466 to activate PI3K/AKT/mTOR signaling and therefore hyperphosphorylating 4E‐BP1, thus promoting the interaction between eIF4E and eIF4G, and resulting in increased FOXD1 protein, and inevitably contributing to GC development and DDP resistance (Fig. 8). Here, MTOR is linked to gastric cancer.